Considering the observed neuroprotective and pro-myelinating effects of the TrkB agonist LM22A-4 in models of demyelination and traumatic brain injury (Fletcher et al., 2021), a promising hypothesis is that targeting TrkB with novel agonists could serve as a drug-based strategy to enhance myelin, complementing amyloid and tau-centered therapies in AD. This evidence concerns the gene NTRK2 and Alzheimer disease.